There is no question that heart function results from the action of heart muscle. Thus, left ventricular, LV, chamber pressure is the result of myocardial force development and LV ejection is the result of myocardial shortening. However, our understanding of how myocardial force and shortening are converted into LV pressure and ejection remains incomplete. Particularly, there is little understanding of how dynamic muscle actions which define instantaneous force-length relations are expressed in the LV to bring about dynamic pressure-volume relations. This understanding is important if modern knowledge of cellular function is to be used for inferring mechanisms responsible for LV function and disfunction. Further, this understanding is key to integrating knowledge obtained at the multiple levels of biological organization in the heart. With the overall objective of bridging the gap between LV chamber and heart muscle dynamic behaviors, a series of experiments are proposed in the isolated rabbit heart and in isolated rabbit heart muscle where the confounding influence of time-varying activation has been removed by creating conditions of constant activation. Identical small-amplitude step and frequency response protocols will be conducted in isolated heart and heart muscle to establish dynamic similarities, dynamic differences and transforming factors by which muscle dynamics are converted into overall ventricular dynamics. Specific hypotheses regarding mechanisms responsible for the mechanical response will be tested including hypotheses relative to variation and time course of stiffness and cross-bridge distortion as components of the mechanical response and to cross-bridge mechanisms that underlie the damped oscillatory component of the mechanical response. An analytical model of cross-bridge mechanisms responsible for dynamic responses will be developed and validated. The analytic model will then be used to evaluate physiological perturbations designed to modify specific components of the response including: initial muscle length, temperature, pH, and level of activation. Finally, a quantitative evaluation of factors causing transformation of elemental contractile dynamics into whole organ left ventricular mechanics will be undertaken.